The aim of this project is to test the hypothesis that ACTH, alone or in conjunction with plasma catecholamines (CA) causes the elevated salt appetite and blood pressue of spontaneously hypertensive (SHR) rats. A two-fold approach will be used. The first will examine whether blood pressure and salt intake of normotensive Wilstar Kyoto (WKY) rats can be elevated by infusing ACTH (and CA) and raising plasma concentration to the levels found in SHR. The second will attempt to reverse or prevent the development of hypertension and high salt appetite in SHR by chronically infusing examethasone, a potent inhibitor of ACTH and beta-endorphin (B-END), the latter of which stimulates the release of adrenal CA. The rats will be fitted with indwelling cathethers in the abdominal aorta and vena cava for monitoring blood pressure, collecting blood samples and infusing drugs. In some rats an osmotic mini-pump inserted under the skin of the neck will be used for infusing ACTH (and B-END) into the lateral cerebral ventricle. Infusion rates are calculated to produce physiological levels of ACTH (and CA), which together with corticosterone and B-END will be measured by radioimmunoassy. Baseline hormone levels, both at rest and under conditions of stress, will be established in experimental and control rats prior to the infusion experiments. Results from this and other labs indicate that compared to WKY, SHR have higher resting levels of ACTH and CA, but not corticosterone, with B-END still to be determined. Salt appetite will be determined by 24-hr 2-bottle preference tests. Conventional electrophysiological recordings will be made to see if the differences in salt preference are mediated by differential responsiveness of the chorda tympani nerve to salt stimulation of the tongue. If successful, these experiments will advance the long-term objectives of understanding the neurobiological mechanisms that underlie salt preference and consumption and how these relate to hypertension. They may show that high blood pressure and high salt consumption are normal consequences of the body's adaptive response to stress and that it may be better policy to change lifestyles rather than improve medication.